Female-limited X-chromosome evolution

Female Drosophila melanogaster.

This project is a follow-up to a previous investigation of male-limited X-chromosome (MLX) evolution in Drosophila melanogaster.
By using an FM balancer chromosome, we have forced the X to only be expressed in females for many generations. This results in a
relaxation of counter-selection in males, and causes the X to evolve to maximize female fitness. The female-limited X-chromosome
evolution (FLX) experiment will therefore help to resolve a number of outstanding questions, for example whether the magnitude of the
response is the same in FLX evolution as in MLX evolution, and whether it is the same traits which respond. Males are generally
expected to be subject to stronger sexual selection than females, so it is possible that both sexes are displaced towards the male
optimum for such traits. In that case we would expect to see a larger change as result of FLX evolution in traits that are sexually
selected in males (but not male-limited in expression) relative to traits that are subject to natural selection in either sex. Another
exciting question which the FLX experiment may be able to shed some light on is the importance and nature of dominance and epistasis
in Drosophila. By expressing evolved X-chromosomes in females in a heterozygous (i.e. one FLX-evolved X-chromosome and one
Control X-chromosome) or homozygous (i.e. two FLX-evolved X-chromosomes) state, we can test for fitness-related dominance and epistatic
variance on the X-chromosome. Theory suggests that dominance should be important for X-linked sexually antagonistic genetic variation,
and results from the MLX experiment suggest that epistatic interactions between the X-chromosome and the autosomes are common for
sexually antagonistic loci.

We have confirmed that FLX females have indeed responded to the selection imposed, by increasing both fecundity and
body size. Males have increased in body size as well, and there is evidence that this change is partly due to coevolution between
the X-chromosome and the autosomes. We are currently investigating the genomic basis of the response to the selection treatment.